The document discusses endometrial cancer. It notes that the incidence is highest among white populations in the US and lowest in India and Japan. Unopposed estrogen stimulation is the main risk factor. Risk increases with late menopause after age 52, obesity, family history of certain cancers, and nulliparity. Symptoms include postmenopausal bleeding, irregular bleeding, and abnormal discharge. Diagnosis involves endometrial biopsy and imaging tests. The cancer spreads locally within the uterus first and then can spread to lymph nodes or distant sites like lungs and liver.

3. The incidence is higher
amongst the white population
of the United States and
lowest in India and Japan.

5. Persistent stimulation of endometrium with unopposed estrogen is
the single most important factor for the development of
endometrial cancer.

6. Postmenopausal with a median age of 60

7. Late menopause—The chance of carcinoma increases, if
menopause fails to occur beyond 52 years.

8. Common in unmarried
In married – asso with nulliparity
Corpus Cancer Syndrome – obesity, HTN, DM

9. Obesity  high free oestradiol  which is
due to decreased SHBG
Unopposed oestrogen stimulation (Ovarian
tumours, PCOS)

10.  Family history or personal history of colon, ovarian or
breast cancer increases the risk of endometrial cancer.

11. Fibroid is associated in about 30 percent cases.
Endometrial hyperplasia precedes carcinoma in about 25 percent
cases.

12. Naked eye—The uterus may be smaller, normal or even enlarged.
Two varieties are found:
Localised  on the fundus  sessile/pendulated. Myometrium
involvement is late.
Diffuse  through endometrium then myometrium (commonly) 
reaches the serosal coat.

13. Adenocarcinoma (endometrioid 80%)
Adenocarcinoma with squamous elements.
 Papillary serous carcinoma (5–10%)
Mucinous adenocarcinoma (5%).
Clear cell adenocarcinoma (5%).
Secretory carcinoma (1%).
Squamous cell carcinoma.
Mixed carcinoma

14. Direct: It is slow growing, it is confined to the stroma for
a long time but eventually, it spreads in all directions.
Thus, it may infiltrate the myometrium and spread to the
parametrium or into the peritoneal cavity.

15. Lymphatic: The lymphatic spread is usually late.
Lymphatic spread involves pelvic, paraaortic (through
infundibulopelvic ligament) and rarely inguinal and
femoral (through lymphatics of round ligament) nodes.

16. Hematogenous: Blood borne spread occurs late. The
common sites of metastases are lungs, liver, bones and
brain.

18. Usually a nullipara, likely to be postmenopausal.
There may be history of delayed menopause.
She may be obese; likely to have hypertension or diabetes

19. Postmenopausal bleeding (75%)
which may be slight,
irregular or continuous.
The bleeding at times may be excessive.

20. In Premenopausal women  irregular & excessive bleeding.
There is watery and offensive discharge due to pyometra.
Pain is common. It may be colicky due to uterine contractions in an
attempt to expel the polypoidal growth.
 Few patients (< 5%) remain asymptomatic.

21.  Speculum examination reveals the cervix looking healthy and the
blood or purulent offensive discharge escapes out of the external os.
 Bimanual examination reveals—The uterus is either atrophic,
normal or may be enlarged due to spread of the tumor, associated
fibroid or pyometra.
 The uterus is usually mobile unless in late stage, when it becomes
fixed.

22.  Endometrial biopsy
 Pap Smear  +ve only in 30%  so not a reliable
 Ultrasound and Colour Doppler  ET, Hyperechoic endometrium with
irregular outline. Increased vascularity. Intrauterine fluid.
 Hysteroscopy  direct visualisation of endometrium and targeted
biopsy
 Fractional Curettage  to know the extent of growth.
 CT scan of abdomen and pelvis  Lymph nodes
 MRI  myometrial invasion
 PET differentiate between normal and cancerous tissue.